Epstein-Barr (EBV) persists as a latent infection in the peripheral blood B lymphocytes. By age 60, greater than 95% of the population has been infected with EBV. The aging immune system manifests signs of progressive deficiency which could lead to a diminished control of EBV. Moreover, aging is a significant risk factor for the emergence of various human malignancies, including B cell lymphomas that are typically associated with EBV. Therefore, we propose that a decreased immune surveillance for EBV in the elderly could lead to increased vial reactivation and viral load which, in turn, could lead to increased viral reactivation and viral load which, in turn, could lead to a heightened potential for EBV-driven lymphomagenesis. We plan to test two basic predicions of this model: i) that T cell-dependent immune responses that control EBV infection are compromised in the elderly and ii) that EBV reactivation and vial load are increased in the elderly.